**5. Face-recognition system in Capgras delusion**

Usually, we do not strive for facial recognition. The ability to identify people who we met before is a headstone of our social interactions. Face recognition is a multistage process ending with the identification of a person. Prosopagnosia is defined as loss of familiarity to previously known faces and the inability to learn to recognize new faces. Although these patients fail to recognize faces, they are still able to show affective responses to these faces [30, 31]. Several studies have suggested that CS represents a 'mirror image' of prosopagnosia, thus suggesting different neural circuits for facial processing: a cognitive circuit (impaired in prosopagnosia) and an affective circuit (impaired in CS). In the affective circuit, the ventral route from the visual centers to the temporal lobes may be protected, also active in conscious face recognition; however, the dorsal visual track that gives the face its emotional significance is damaged. A brief disruption of the ventral visual pathway leads to prosopagnosia, whereas damage to the dorsal visual areas leads to an impaired sense of familiarity for known faces, as in CS [9, 17, 30, 32]. While the ability to identify that person is intact, patient with CS probably has a brain lesion that interferes with the patient's ability to sense a familiarity toward the significant other [15]. It has been suggested that the impairment seen in the Capgras delusion was linked to a disruption of pathways connecting face-sensitive regions to limbic cortex, which is involved in the accompanying emotional response [30]. Perhaps arising from the conflicting experience of recognizing a known face without any accompanying affective reaction, the patient can understand that the absence of this emotional arousal is to establish the belief that the person he is looking at is an imposter [9, 33]. In another connectivity study, posterior coupled with anterior right hemisphere dysfunction may have involved in the emergence of Capgras delusion [34]. Also, it has been suggested that CS results from the disconnection of the face processing regions in the inferior temporal lobe from structures in the limbic system, especially the amygdala, which is very important in assigning emotional value to familiar faces [34]. Common to the CS is a fixed false belief but infrequently transient [35]. However, anatomical disconnection models fail to efficiently consider the transient nature of the misidentification episodes [34]. Therefore, it has been suggested that CS may be associated with the 'kindling of subcortical structures'. Kindling refers to repeated subthreshold stimuli which may result in psychomotor outbursts or overt seizure activity [34]. Autonomic responses and eye movements are involved in face perception which may cause the patient believe that the person has been replaced by an imposter. Studies on patient with CS like other psychiatric disorders have shown abnormal scan paths to facial stimuli or abnormal skin conductance response (SCR) in face processing tasks [30, 33]. The absence of identity recognition, accompanied by a lack of SCR, stimulates the patient to explore unfamiliar faces, and identity recognition of familiar faces leads to a more detailed exploration in the eye region, and it results in gaze avoidance of the eye region [33]. Vision is important in accessing reserved knowledge in the etiology of CS. However, surprisingly CS has also been reported in a number of blind patients which suggests that it cannot have an exclusively visual basis [34]. Some theories assume that two deficits are necessary for delusions to occur in the case of Capgras delusion like other DMSs [32, 36]. This is also called 'two-hit' process [20]. The first one, the brain's ability to attach emotional emphasis, may be the lack of autonomic arousal which leads to the abductive inference that the person is an imposter [30]. The other deficit is an impaired ability to reassess beliefs [the global consistency-checking mechanism] which prevents the rejection of the bizarre belief. The second deficit leads to the persistence of that abnormal perception as a delusion resistant to reasoning, also related to the right anterior cortex of the second deficit [9, 30, 32, 36].
